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Alpha-4 integrins and VCAM-1, but not MAdCAM-1, are essential for recruitment of mast cell progenitors to the inflamed lung
- Abonia, J Pablo (author)
-
- Hallgren, Jenny (author)
- Harvard Medical School, Boston, MA
- Jones, Tatiana (author)
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- Shi, Tong (author)
- Xu, Yuhui (author)
- Koni, Pandelakis (author)
- Flavell, Richard A (author)
- Boyce, Joshua A (author)
- Austen, K Frank (author)
- Gurish, Michael F (author)
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- (creator_code:org_t)
- American Society of Hematology, 2006
- 2006
- English.
- In: Blood. - : American Society of Hematology. - 0006-4971 .- 1528-0020. ; 108:5, s. 1588-1594
- Journal article (peer-reviewed)
Abstract
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- Normal mouse lungs lack appreciable numbers of mast cells (MCs) or MC progenitors (MCp's), yet the appearance of mature MCs in the tracheobronchial epithelial surface is a characteristic of allergic, T-cell-dependent pulmonary inflammation. We hypothesized that pulmonary inflammation would recruit MCp's to inflamed lungs and that this recruitment would be regulated by distinct adhesion pathways. Ovalbumin-sensitized and challenged mice had a greater than 28-fold increase in the number of MCp's in the lungs. In mice lacking endothelial vascular cell adhesion molecule 1 (VCAM-1) and in wild-type mice administered blocking monoclonal antibody (mAb) to VCAM-1 but not to mucosal addressin CAM-1 (MadCAM-1), recruitment of MCp's to the inflamed lung was reduced by greater than 75%. Analysis of the integrin receptors for VCAM-1 showed that in beta7 integrin-deficient mice, recruitment was reduced 73% relative to wild-type controls, and in either BALB/c or C57BL/6 mice, mAb blocking of alpha4, beta1, or beta7 integrins inhibited the recruitment of MCp's to the inflamed lung. Thus, VCAM-1 interactions with both alpha4beta1 and alpha4beta7 integrins are essential for the recruitment and expansion of the MCp populations in the lung during antigen-induced pulmonary inflammation. Furthermore, the MCp is currently unique among inflammatory cells in its partial dependence on alpha4beta7 integrins for lung recruitment.
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